Not selling anything, just something that surprised me when I actually did the math.

Typical day for a lot of us: eggs, whey, chicken-rice, paneer, maybe a protein bar. Eggs, whey, chicken and paneer all have zero fibre. White rice has almost none. When I counted a day like that, it came to around 10–14g of fibre. Most guidelines say adults need 25–40g.

Why it matters: when there isn’t much fibre, more undigested protein reaches your colon and gut bacteria ferment that instead. That tends to bring the smelly gas and heavy feeling.

Other things worth ruling out first:

• Whey concentrate still has some lactose. Try isolate for 2 weeks.
• Protein bars with maltitol/sorbitol are notorious for gas.
• Chugging shakes fast means swallowing air.

What helped:

• Swapping half the rice for rajma/chana/masoor (more fibre AND more protein)
• 1 fruit a day with skin on (guava is great)
• A spoon of oats or chia in the post-workout shake
• Going SLOW. Add 3–5g every few days, or you’ll bloat more and give up.

Has anyone else tracked fibre alongside protein? Curious what your numbers looked like.

Abstract

• PMID: 42012901

Acesulfame K (Ace-K) is a commonly consumed sweetener, although knowledge about the Ace-K-gut microbiota interaction remains limited. This study evaluates dose-dependent effects of Ace-K on metataxonomics, metagenomics, and metabolic activity of children gut microbiota developed in a dynamic gut simulator. An Ace-K-dose dependent increase in Anaerostipes, Coprococcus, Subdoligranulum, Blautia, Sutterella wadsworthensis, Alistipes, and Bacteroides thetaiotaomicron was observed. Butyrate showed a dose-response increase that correlated with Ace-K consumption, suggesting its microbial metabolism. Increasing bacterial taxa showed sulfatase and amidase activities potentially capable of degrading Ace-K, releasing sulfamate and acetoacetate, which species such as Anaerostipes hadrus and Intestinimonas can metabolize to produce butyrate via the butanoyl-CoA pathway. Furthermore, the Ace-K-microbiome interaction led to a dose-dependent decrease in Caco-2 epithelial integrity, possibly due to the release of sulfated metabolites. This study provides evidence of the potential risk of Ace-K consumption based on its metabolism by the human gut microbiome.

TL;DR

"The findings suggest berries containing high levels of polyphenols may improve vascular function in both the micro- and microvasculature. However, the supplementation protocol (ie, single dose vs multiple dose) appears to have a more pronounced effect on microvascular function."

Abstract

Context: Several studies have investigated the effect of berries high in polyphenol content on vascular function. Polyphenols have antioxidant properties and enhance nitric oxide bioavailability. However, existing reviews investigated the effects of polyphenols on vascular health without distinguishing between micro- and macrovascular function.

Objectives: This review explores the impact berries high in polyphenols (containing ≥200 mg of total polyphenols per 100 g or 100 mL) on macro- and microvascular function to better understand their role in vascular health.

Data source: A systematic search was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines across the PubMed, SciELO, and Web of Science databases using the following combined keywords: ("Berries" OR "Polyphenol-rich foods" OR "Polyphenols") AND ("Arterial stiffness" OR "Blood flow" OR "Macrovascular function" OR "Microcirculation" OR "Vascular function").

Data extraction: Randomized controlled trials evaluating the effects of polyphenols derived from berries on macro- and microvascular function were included. Data extraction was performed independently by 2 researchers, and the risk of bias was assessed using the Cochrane risk-of-bias tool.

Data analysis: A total of 35 studies were included and analyzed. Among these, 26 studies evaluated the effects of polyphenols from berries on macrovascular function, 6 studies evaluated their effects on microvascular function, and 3 studies examined both macro- and microvascular function.

Conclusion: The findings suggest berries containing high levels of polyphenols may improve vascular function in both the micro- and microvasculature. However, the supplementation protocol (ie, single dose vs multiple dose) appears to have a more pronounced effect on microvascular function.

https://pubmed.ncbi.nlm.nih.gov/41183514/

Weight loss during intermittent fasting, not Mediterranean diet quality alone, is associated with lower inflammation: A randomized controlled trial

DOI: https://doi.org/10.1016/j.cmet.2026.09.017

Abstract

Low-grade inflammation is a significant contributor to various chronic diseases, including cardiometabolic disorders. While the Mediterranean diet has been linked to reduced inflammation, it is unclear whether this effect is due to the diet's quality or the weight loss often associated with it. This study aimed to dissect the independent effects of the Mediterranean diet and intermittent fasting on inflammation among adults with metabolic risk factors. The trial involved 53 participants (77% female, mean age 54.7 years) who were randomized to either a Mediterranean diet or their habitual Western diet for eight weeks, followed by an eight-week phase of intermittent fasting.

The primary outcome, high-sensitivity C-reactive protein (hsCRP), showed no significant change during the diet-only phase (p = 0.394), indicating that diet quality alone did not reduce inflammation. However, during the fasting phase, hsCRP levels decreased significantly in the Mediterranean group by 0.29 mg/L (95% CI: -0.50, -0.09; p < 0.01), corresponding to a 25% reduction from baseline. Participants in the Mediterranean diet lost an average of 3.63 kg (95% CI: -4.51, -2.78) compared to 1.88 kg (95% CI: -2.51, -1.29) in controls, highlighting that weight loss during intermittent fasting was the key driver of reduced inflammation.

Study Design and Methodology

• Sample Size: N = 53 participants
• Duration: 16 weeks
• Measurement Tools: High-sensitivity C-reactive protein (hsCRP), dual-energy X-ray absorptiometry (DEXA) for body composition, 4-day weighed food records for dietary adherence.
• Controls Used: Participants in the control group continued their habitual Western diet.
• Metabolic Ward: Yes, controlled feeding was implemented.
• Blinding: No blinding was reported.
• Washout Period: Not applicable, as the study was designed in two phases without a washout.

Key Findings

• hsCRP did not change significantly during the diet-only phase (p = 0.394).
• During the fasting phase, hsCRP decreased by 0.29 mg/L (p < 0.01) in the Mediterranean group.
• Weight loss in the Mediterranean group was 3.63 kg (95% CI: -4.51, -2.78) compared to 1.88 kg (95% CI: -2.51, -1.29) in controls (p < 0.01).
• Triglycerides decreased by 22% in the Mediterranean group during the initial phase.
• Total and LDL cholesterol declined further during the fasting phase but without significant differences between groups.

Limitations

• Small sample size limits generalizability.
• Self-reporting of dietary intake may introduce bias.
• Short follow-up period may not capture long-term effects.
• High dropout rates, with only 43 completing the study.
• Lack of blinding could affect the perceived outcomes.

Discussion and Implications

This study provides crucial insights into the relationship between diet, weight loss, and inflammation. It clarifies that while the Mediterranean diet can improve lipid profiles, its anti-inflammatory effects are primarily linked to weight loss achieved through intermittent fasting rather than the diet itself. This finding has significant implications for dietary guidelines and public health policy, suggesting that strategies focusing on energy deficit and weight management may be more effective in reducing inflammation than dietary quality alone.

Moreover, when individuals transition to diets emphasizing whole foods and minimizing processed options, weight loss often becomes a critical factor. Such dietary changes typically lead to a natural caloric deficit, as these diets are generally lower in calories yet higher in nutrient density. This not only supports metabolic health but also promotes satiety, making it easier for individuals to lose weight. The behavioral shift that accompanies a focus on whole foods can result in healthier eating patterns and a greater awareness of food choices, further aiding in weight loss and improved health outcomes.

The findings from this study emphasize the importance of considering both dietary composition and energy balance in nutritional interventions. While the Mediterranean diet has its benefits, the broader implications suggest that the reduction of processed foods and an increase in whole food consumption can be powerful drivers of weight loss and improved health. This perspective aligns with emerging trends in nutrition science, which advocate for less processed and more whole food diets as a means to combat chronic diseases linked to inflammation and metabolic dysfunction.

In summary, this study emphasizes the importance of weight loss in reducing inflammation rather than solely relying on diet quality. More research is needed to fully understand the mechanisms at play and to refine dietary recommendations for improving health outcomes.

TL;DR:

• Ketogenic diet in this context: 4:1 ratio = 80% fat.

• Modified Atkins: 10-20 g carbs but no set fat/protein ratio, the goal is still to achieve ketosis.

Both diets have been shown to be effective in reducing seizure frequency in children with drug-resistant epilepsy. However, the modified Atkins diet is generally less restrictive and easier to maintain than the classic ketogenic diet.

Abstract

Importance: Despite advances in the understanding of dietary therapies in children with drug-resistant epilepsy, no quantitative comparison exists between different dietary interventions.

Objective: To evaluate the comparative efficacy and safety of various dietary therapies in childhood drug-resistant epilepsy.

Data sources: Systematic review and network meta-analysis (frequentist) of studies in PubMed, Embase, Cochrane, and Ovid published from inception to April 2022 using the search terms ketogenic diet, medium chain triglyceride diet, modified Atkins diet, low glycemic index therapy, and refractory epilepsy.

Study selection: Randomized clinical trials comparing different dietary therapies (ketogenic diet, modified Atkins diet, and low glycemic index therapy) with each other or care as usual in childhood drug-resistant epilepsy were included. Abstract, title, and full text were screened independently by 2 reviewers.

Data extraction and synthesis: Data extraction was conducted following Preferred Reporting Items for Systematic Reviews and Meta-analyses reporting guideline. Cochrane risk-of-bias tool was used to assess the study quality. Effect sizes were calculated as odds ratio with 95% CI using random-effects model. The hierarchy of competing interventions was defined using the surface under the cumulative ranking curve.

Main outcomes and measures: Short-term (≤3 months) 50% or higher and 90% or higher reduction in seizure frequency and treatment withdrawal due to adverse events were the primary efficacy and safety outcomes.

Results: Of 2158 citations, 12 randomized clinical trials (907 patients) qualified for inclusion. In the short term, all dietary interventions were more efficacious than care as usual for 50% or higher seizure reduction (low glycemic index therapy: odds ratio [OR], 24.7 [95% CI, 5.3-115.4]; modified Atkins diet: OR, 11.3 [95% CI, 5.1-25.1]; ketogenic diet: OR, 8.6 [95% CI, 3.7-20.0]), while ketogenic diet (OR, 6.5 [95% CI, 2.3-18.0]) and modified Atkins diet (OR, 5.1 [95% CI, 2.2-12.0]) were better than care as usual for seizure reduction of 90% or higher. However, adverse event-related discontinuation rates were significantly higher for ketogenic diet (OR, 8.6 [95% CI, 1.8-40.6]) and modified Atkins diet (OR, 6.5 [95% CI, 1.4-31.2]) compared with care as usual. Indirectly, there was no significant difference between dietary therapies in efficacy and safety outcomes.

Conclusions and relevance: This study found that all dietary therapies are effective in the short term. However, modified Atkins diet had better tolerability, higher probability for 50% or higher seizure reduction, and comparable probability for 90% or higher seizure reduction and may be a sounder option than ketogenic diet. Direct head-to-head comparison studies are needed to confirm these findings.

https://pubmed.ncbi.nlm.nih.gov/36716045/

TL;DR

"Daily unprocessed beef intake do not significantly affect most blood lipids, apolipoproteins, or blood pressures, except for a small increase in LDL-cholesterol compared with diets with less or no beef. Thus, there may be other factors influencing the association of red meat and beef on CVD risk that deserve further investigation."

Abstract

Background: Results from observational studies suggest associations of red meat intake with increased risk of cardiovascular disease (CVD); however, RCTs have not clearly demonstrated a link between red meat consumption and CVD risk factors. Further, the specific effects of beef, the most consumed red meat in the United States, have not been extensively investigated.

Objectives: This study aimed to perform a systematic review and meta-analysis of RCT data evaluating the effects of minimally or unprocessed beef intake on CVD risk factors in adults.

Methods: A search of the literature was conducted using PubMed and CENTRAL databases. RCTs in adults that provided diets with fresh or minimally processed beef were included. Data were extracted, and pooled estimates from random-effects models were expressed as standardized mean differences (SMDs) between the beef intervention and comparator intervention with less or no beef. Sensitivity and subgroup analyses were also performed.

Results: Twenty relevant RCTs that met the criteria were included. Beef intake did not impact blood pressure or most lipoprotein-related variables, including total cholesterol, HDL-cholesterol, triglycerides, non-HDL-cholesterol, apolipoprotein A or B, and VLDL-cholesterol. Beef consumption had a small but significant effect on LDL-cholesterol (0.11; 95% CI: 0.008, 0.20; P = 0.03), corresponding to ∼2.7 mg/dL higher LDL-cholesterol in diets containing more beef than that in low-beef or -o beef comparator diets. Sensitivity analyses show this effect was lost when 1 influential study was removed.

Conclusions: Daily unprocessed beef intake do not significantly affect most blood lipids, apolipoproteins, or blood pressures, except for a small increase in LDL-cholesterol compared with diets with less or no beef. Thus, there may be other factors influencing the association of red meat and beef on CVD risk that deserve further investigation.

https://pubmed.ncbi.nlm.nih.gov/39649475/

For example, I would always eat eggs and nuts before the tomatoes, so I’d always have the fat overflowing in my belly anyway.

Do we still need to add fat (olive oil, butter, etc.) in the middle of heating the tomatoes (i.e. stir-frying) or after, in this situation?

Any scientific difference in bioavailability between fat pre-absorbed in the tomato cells vs. fat mixed in the body?

(I want to save calories if it’s unnecessary)

Hi all! I am a PhD student in my 2nd Year studying nutritional and cognition, mood and blood markers (specifically fermented dairy). I am using the 3FQ fermented food frequency questionnaire (https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2025.1667653/full) in my research, but due to accessibility to portion size photos, I am not able to capture the data where ppts choose their intake of foods based on a portion estimate photographs. Is there any advice on how to analyse this data? I have the frequency responses, and I am also completing the EPIC FFQ questionnaire. Thank you!

1) I'm thinking about gaining some weight. Are there any specific considerations for gym workouts—aimed at weight gain—given my gene mutations? (I'm particularly interested in the topics of recovery, compound/basic exercises, and training "to failure")

2) Is there an approximate daily limit for methionine intake, given my gene mutations, or am I free to consume as much methionine as I like?